{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,12]],"date-time":"2026-05-12T13:17:17Z","timestamp":1778591837453,"version":"3.51.4"},"reference-count":71,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>\n                    Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) remains a major cause of short-term mortality, yet its biological drivers are incompletely understood. Increasing evidence indicates that the distal lung is not sterile and that microbial burden, ecological disruption, and host immune responses may interact within the fibrotic niche. Here, we summarize current evidence and propose a focused, hypothesis-generating framework for microbiome-immune crosstalk in AE-IPF. In this model, pulmonary dysbiosis and persistent microbial stimulation may converge with epithelial injury-derived danger signals to amplify pattern-recognition receptor signaling, reshape macrophage states, and promote injurious neutrophil responses, including excessive neutrophil extracellular trap formation. Emerging data from fibrotic lung disease also raise the possibility that SPP1-associated macrophage programs may contribute to both impaired host defense and maladaptive repair. These observations also support the view that immune-cell state transitions, rather than microbial burden alone, may shape how acute injury is translated into persistent fibroinflammatory remodeling. We also discuss how antimicrobial exposure and resistance-associated persistence traits, including biofilm formation, could contribute to impaired microbial clearance and sustained innate immune activation, while emphasizing that direct\n                    <jats:italic>in situ<\/jats:italic>\n                    evidence in AE-IPF remains limited. Rather than proposing a universal mechanism, this mini review highlights a testable amplification framework that may help refine pathogen-aware stratification, antimicrobial stewardship, and biomarker-guided host-directed strategies in future studies.\n                  <\/jats:p>","DOI":"10.3389\/fimmu.2026.1847027","type":"journal-article","created":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T04:18:15Z","timestamp":1777609095000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Microbiome-innate immune crosstalk in acute exacerbation of idiopathic pulmonary fibrosis: an amplification framework"],"prefix":"10.3389","volume":"17","author":[{"given":"Wanwan","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wannan Medical University","place":["Wuhu, Anhui, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiayang","family":"Yi","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, The First Affiliated Hospital of Wannan Medical University","place":["Wuhu, Anhui, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhi","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Rheumatology, The First Affiliated Hospital of Wannan Medical University","place":["Wuhu, Anhui, China"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,1]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1183\/13993003.00419-2015","article-title":"Acute exacerbation of idiopathic pulmonary fibrosis: shifting the paradigm","volume":"46","author":"Ryerson","year":"2015","journal-title":"Eur Respir J"},{"key":"B2","doi-asserted-by":"publisher","first-page":"8710","DOI":"10.1038\/s41467-025-63735-1","article-title":"Aberrant intermediate alveolar epithelial cells promote pathogenic activation of lung fibroblasts in preclinical fibrosis models","volume":"16","author":"Hoffman","year":"2025","journal-title":"Nat Commun"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.3389\/fphar.2023.1205948","article-title":"Progress in understanding and treating idiopathic pulmonary fibrosis: recent insights and emerging therapies","volume":"14","author":"Guo","year":"2023","journal-title":"Front Pharmacol"},{"key":"B4","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbadis.2024.167572","article-title":"Integrated multiomic analysis identifies TRIP13 as a mediator of alveolar epithelial type II cell dysfunction in idiopathic pulmonary fibrosis","volume":"1871","author":"St Pierre","year":"2025","journal-title":"Biochim Biophys Acta Mol Basis Dis"},{"key":"B5","doi-asserted-by":"publisher","first-page":"415","DOI":"10.1186\/s12931-024-03048-x","article-title":"Acute exacerbation of progressive pulmonary fibrosis: incidence and outcomes","volume":"25","author":"Kim","year":"2024","journal-title":"Respir Res"},{"key":"B6","doi-asserted-by":"publisher","first-page":"296","DOI":"10.1186\/s12931-023-02595-z","article-title":"Animal models of acute exacerbation of pulmonary fibrosis","volume":"24","author":"Ye","year":"2023","journal-title":"Respir Res"},{"key":"B7","doi-asserted-by":"publisher","DOI":"10.7759\/cureus.22606","article-title":"Acute exacerbation of idiopathic pulmonary fibrosis with pirfenidone and nintedanib: a friend or foe","volume":"14","author":"Kaushal","year":"2022","journal-title":"Cureus"},{"key":"B8","doi-asserted-by":"publisher","DOI":"10.1164\/rccm.202001-0057ED","article-title":"Treatment of acute exacerbation of idiopathic pulmonary fibrosis. 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